In patients that suffered from neuronal damages, whether traumatic, inflammatory, infectious, tumor-related, ischemic, degenerative, metabolic or toxic, often secondary neuronal damages, such as cellular death and chronic pain, in particular neuropathic pain, take place as a cause of these neuronal damages.
Neuropathic pain can emerge from manifold damages of peripheral and central neuronal cells Pain is common in, amongst others, diabetic or toxic (such as, for example, due to a chemotherapeutical therapy) polyneuropathy, phantom pains following amputation, postzosteric neuralgia, trigeminus neuralgia, compression syndrome, such as the carpal tunnel syndrome, and ischialgia in spinal prolapse, pain in multiple sclerosis and post-ischemic neuralgia. The non-invasive medicamentous possibilities that are known from the state of the art are limited to the use of different antiepileptics (e.g. gabapentin, pregabalin), anti-depressives (e.g. amitrytilin) and opioids, which, nevertheless, can only achieve a sufficient analgetic effect with simultaneously tolerable side effects in only about 30% of the patients, and do not influence the neuronal damage.
The mechanisms that contribute to the generation of chronic, in particular neuropathic, pain are diverse. Experimental studies in recent years show that the transsynaptic destruction of inhibitory neurons and the activation of glial cells essentially add to this.
Accordingly, it is an object of the present invention to provide a method or a means, respectively, which can be used for the therapy or prophylaxis of a neuronal damage, in order to particularly favour the regeneration in partially peripheral neuronal lesions, and to prevent the secondary cellular death.